3km9

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[[Image:3km9.png|left|200px]]
 
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{{STRUCTURE_3km9| PDB=3km9 | SCENE= }}
{{STRUCTURE_3km9| PDB=3km9 | SCENE= }}
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===Structure of complement C5 in complex with the C-terminal beta-grasp domain of SSL7===
===Structure of complement C5 in complex with the C-terminal beta-grasp domain of SSL7===
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{{ABSTRACT_PUBMED_20133685}}
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==Disease==
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[[http://www.uniprot.org/uniprot/CO5_HUMAN CO5_HUMAN]] Defects in C5 are the cause of complement component 5 deficiency (C5D) [MIM:[http://omim.org/entry/609536 609536]]. A rare defect of the complement classical pathway associated with susceptibility to severe recurrent infections, predominantly by Neisseria gonorrhoeae or Neisseria meningitidis. Note=An association study of C5 haplotypes and genotypes in individuals with chronic hepatitis C virus infection shows that individuals homozygous for the C5_1 haplotype have a significantly higher stage of liver fibrosis than individuals carrying at least 1 other allele (PubMed:15995705).
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==Function==
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[[http://www.uniprot.org/uniprot/CO5_HUMAN CO5_HUMAN]] Activation of C5 by a C5 convertase initiates the spontaneous assembly of the late complement components, C5-C9, into the membrane attack complex. C5b has a transient binding site for C6. The C5b-C6 complex is the foundation upon which the lytic complex is assembled. Derived from proteolytic degradation of complement C5, C5 anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes. C5a also stimulates the locomotion of polymorphonuclear leukocytes (chemokinesis) and direct their migration toward sites of inflammation (chemotaxis).
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(as it appears on PubMed at http://www.pubmed.gov), where 20133685 is the PubMed ID number.
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{{ABSTRACT_PUBMED_20133685}}
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==About this Structure==
==About this Structure==
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3KM9 is a 4 chains structure with sequences from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Staphylococcus_aureus_subsp._aureus_str._newman Staphylococcus aureus subsp. aureus str. newman]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KM9 OCA].
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[[3km9]] is a 4 chain structure with sequence from [http://en.wikipedia.org/wiki/Homo_sapiens Homo sapiens] and [http://en.wikipedia.org/wiki/Staphylococcus_aureus_subsp._aureus Staphylococcus aureus subsp. aureus]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=3KM9 OCA].
==Reference==
==Reference==
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<ref group="xtra">PMID:20133685</ref><references group="xtra"/>
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<ref group="xtra">PMID:020133685</ref><references group="xtra"/><references/>
[[Category: Homo sapiens]]
[[Category: Homo sapiens]]
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[[Category: Staphylococcus aureus subsp. aureus str. newman]]
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[[Category: Staphylococcus aureus subsp. aureus]]
[[Category: Andersen, G R.]]
[[Category: Andersen, G R.]]
[[Category: Bjerre, M.]]
[[Category: Bjerre, M.]]
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[[Category: Membrane attack complex]]
[[Category: Membrane attack complex]]
[[Category: Ob-fold]]
[[Category: Ob-fold]]
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[[Category: Polymorphism]]
 
[[Category: Secreted]]
[[Category: Secreted]]
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''Page seeded by [http://oca.weizmann.ac.il/oca OCA ] on Thu Feb 25 09:21:17 2010''
 

Revision as of 21:29, 24 March 2013

Template:STRUCTURE 3km9

Contents

Structure of complement C5 in complex with the C-terminal beta-grasp domain of SSL7

Template:ABSTRACT PUBMED 20133685

Disease

[CO5_HUMAN] Defects in C5 are the cause of complement component 5 deficiency (C5D) [MIM:609536]. A rare defect of the complement classical pathway associated with susceptibility to severe recurrent infections, predominantly by Neisseria gonorrhoeae or Neisseria meningitidis. Note=An association study of C5 haplotypes and genotypes in individuals with chronic hepatitis C virus infection shows that individuals homozygous for the C5_1 haplotype have a significantly higher stage of liver fibrosis than individuals carrying at least 1 other allele (PubMed:15995705).

Function

[CO5_HUMAN] Activation of C5 by a C5 convertase initiates the spontaneous assembly of the late complement components, C5-C9, into the membrane attack complex. C5b has a transient binding site for C6. The C5b-C6 complex is the foundation upon which the lytic complex is assembled. Derived from proteolytic degradation of complement C5, C5 anaphylatoxin is a mediator of local inflammatory process. It induces the contraction of smooth muscle, increases vascular permeability and causes histamine release from mast cells and basophilic leukocytes. C5a also stimulates the locomotion of polymorphonuclear leukocytes (chemokinesis) and direct their migration toward sites of inflammation (chemotaxis).

About this Structure

3km9 is a 4 chain structure with sequence from Homo sapiens and Staphylococcus aureus subsp. aureus. Full crystallographic information is available from OCA.

Reference

  • Laursen NS, Gordon N, Hermans S, Lorenz N, Jackson N, Wines B, Spillner E, Christensen JB, Jensen M, Fredslund F, Bjerre M, Sottrup-Jensen L, Fraser JD, Andersen GR. Structural basis for inhibition of complement C5 by the SSL7 protein from Staphylococcus aureus. Proc Natl Acad Sci U S A. 2010 Feb 4. PMID:20133685

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